Molecular Therapy — Nucleic Acids · 2020 · 93 citations · 31 references
MedicineMolecular BiologyOncologyGene ExpressionMolecular OncologyTumor ProgressionCancer Cell SignalingCancer GenomicsCancer ProgressionCancer TranscriptomicsMolecular Tumor ProfilingOvarian CancerCancer Signaling PathwaysMessenger Rna Binding ProteinsOvarian Cancer MetastasisOvarian Cancer PathogenesisPost-transcriptional RegulationTranscriptional Dysregulation In CancerTranscriptional Repression MechanismsTumor Cell Survival Pathways
. CELF2 expression increased the stability of its target, FAM198B, by binding to AU/U-rich elements (AREs) in the 3' untranslated region (3' UTR). FAM198B knockdown restored the CELF2-mediated suppression of proliferation and migration. We also found that CELF2/FAM198B may repress ovarian cancer progression by inhibiting the mitogen-activated protein kinase/extracellular-regulated protein kinase (MAPK/ERK) signaling pathway. Finally, a curcumin-induced increase in CELF2 expression resulted in increased ovarian cancer cell sensitivity to cisplatin. Our study elucidated a novel mechanism by which the CELF2/FAM198B axis regulates proliferation and metastasis in ovarian cancer, providing novel, potential therapeutic targets for ovarian cancer.
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